A novel α Globin Gene Cluster Duplication, αααα380 Heterozygous ß0-Thal Variant, Leading to a Blood Transfusion-Dependent Phenotype.

To assess the effectiveness of three-level prevention and control of thalassemia, we routinely collect samples from transfusion-dependent individuals and perform genetic analysis. Here, we report on a 10-year-old boy requiring blood transfusions with routine thalassemia gene test results of αα/αα, and ßCD41/42/ßN, but he had thalassemia-like changes in his appearance and a high need for frequent blood transfusions, suggesting a case of thalassemia major in childhood. Given these equivocal results, samples from the family members were collected for further analysis. A multiplex ligation-dependent probe amplification assay was used to detect a multicopy number variant of the α globin gene cluster in the proband. The variant was detected as a long fragment repeat of 380 Kb using CNV assay technique, which contains the entire α globin gene cluster, describing it as αααα380/αα. Analysis of family members suggested that both the brother and mother of the proband carried the variant, and both MCV and MCH values were reduced in carriers. Individuals carrying multiple copy number variants of the α globin gene cluster exist in the population. Individuals carrying such variants who are also heterozygous for the ß0 thalassemia variant result in an imbalance in the α/ß chain ratio, potentially leading to the creation of individuals with a severe anemia genotype. Most secondary prevention and control laboratories currently do not include variants with increased α gene copy number in their testing, which is one of the blind spots of prevention and control efforts. In order to provide more accurate genetic counseling to test subjects, especially in regions with high rates of thalassemia carriage, testing laboratories should pay attention to individual genotype-phenotype matches to avoid the under-detection of such variants.

Identification of the ß thalassemia allele ß-50 and analysis of the hematology data of carriers in a southern Chinese population.

During a routine test, we identified a 38-year-old man who had a positive hematology screening result but was negative for hot spot variants of his thalassemia gene. Further analysis identified ß-50 (HBB: c.-100G>A). It was first suggested that ß-50 was a ß+ -thal allele, and some research groups suggested this allele was a silent ß-thal allele. To fully understand the hematological phenotype of the ß-50 allele, we screened for individuals carrying ß-50 in the general population and performed hematology analysis on these carriers. A real-time PCR detection system was designed to verify samples carrying ß-50 . Twenty-one thousand samples and 43 pedigree samples were screened, and 86 ß-50 carriers were detected. We performed hematological analysis on 65 individuals older than 3 years who had normal serum ferritin and analyzed the data. A total of 34.62% of the ß-50 /ßN individuals had mean cellular volume (MCV) or mean cellular hemoglobin (MCH) values slightly lower than the positive cutoff value of screening; the ß-50 carriers' Hb A2 value was slightly elevated. According to the test results, ß-50 carriers have slight changes in hematology parameters, including slight decreases in MCV and MCH and slight increases in Hb A2 ; however, these effects do not reach the degree of traditional ß+ alleles. Females with genotype ß-50 /ß0 show a degree of decline in hematological indicators during pregnancy. Therefore, we should describe ß-50 as a ß++ thalassemia allele, and identification of ß-50 can explain slight changes in hematological indicators in some carriers.

Identification of Three Families Carrying Hb Anti-Lepore Hong Kong Variant in Guangxi, China, and Analysis of Their Hematological Data.

Thalassemia is a single-gene genetic disease with a high incidence in southern China. To prevent and control thalassemia, the most commonly used procedure is hematology testing and hemoglobin (Hb) analysis, followed by thalassemia gene analysis in positive individuals. During routine testing for thalassemia, we identified three individuals with Hb A2 levels of >10.0%. The results of conventional thalassemia gene analysis of these individuals cannot explain this feature, and there is a possibility of carrying novel thalassemia gene variants. Therefore, we collected samples from these three families for further analysis of the thalassemia gene. The research team used multiplex ligation-dependent probe amplification (MLPA) to analyze the three families, and the analysis results showed that their molecular biological characteristics were similar to those of Hb Anti-Lepore Hong Kong (NG_000007.3: g.63210_70621dup). Then, gap-polymerase chain reaction (gap-PCR) and sequencing methods were used for verification, and it was confirmed that the variant carried by these three families was indeed Hb Anti-Lepore Hong Kong. Three individuals carrying both the - -SEA (Southeast Asian) and Hb Anti-Lepore Hong Kong variants were also detected in this study, and these individuals had slightly lower Hb A2 results than those carrying Hb Anti-Lepore Hong Kong alone. Further analyses revealed that the carrier rate of this variant is about 0.03% in the population, thus identifying it as a rare variant.

Identification of Three Types of α-Thalassemia Deletion, -α21.9, -α2.4, and - -THAI, and Their Frequencies, in One Family in the Population of Southern Guangxi Zhuang Autonomous Region, People's Republic of China.

Different types of deletional α-thalassemia (α-thal) have been reported by researchers in China. This study describes one family carrying -α21.9 (NG_000006.1: g.14373_36299delinsGGGAAGGGTGGGTGGGAATAACAGCTTTT), -α2.4 (NG_000006.1: g.36860_39251del) and - -THAI (Thailand) (NG_000006.1: g.10664_44164del) alleles in Guangxi Zhuang Autonomous Region, People's Republic of China (PRC), and reports the frequencies of these types in the population of this region. The proband was a 4-year-old girl, who screened positive for thalassemia, although the thalassemia genotype results were normal when screened using the routine kits. Samples of the proband's parents were also collected to perform further analyses. Two real-time gap-polymerase chain reaction (gap-PCR) systems were designed for separate detection of - -THAI and screening for -α21.9 and -α2.4. The genotype of the proband was -α21.9/-α2.4, and the two variants were inherited from her parents. In the frequency study, five - -THAI, four -α21.9 and 11 -α2.4 positive individuals were detected in the 3410 random samples. Thus, allele frequencies of -α21.9, - -THAI and -α2.4 in the population of southern Guangxi were determined as 0.059, 0.073 and 0.161%, respectively. This is the first report of an individual carrying the -α21.9/-α2.4 genotype, and the first report of the detection of -α21.9, -α2.4 and - -THAI in a single family. The total frequency for these alleles was 0.293% in southern Guangxi, suggesting that the thalassemia clinical center in this region should utilize a screening kit that allows detection of these types of deletions for a more comprehensive evaluation of thalassemia risk.

Engaging More Nurses in Cancer Preventive Care: Challenges and Opportunities.

EXECUTIVE SUMMARY: Nurse-led care is crucial to improving the effectiveness of cancer prevention, as demonstrated by research. However, barriers to nurse-led cancer preventive care are still prevalent. What are the challenges that impede nurses from providing effective preventive care? How can hospital leaders address these challenges to better engage nurses in preventive care? What should be the focal areas in terms of policy changes and training programs? This article explores those questions. We examine the difficulties nurses have encountered. We identify the barriers yet to be examined extensively. Finally, we propose that many barriers can be addressed through carefully designed nurses' training programs and substantial policy changes. Our data were collected from a Nurse Oncology Education Program survey that included questions on perceived oncology knowledge, current cancer-related preventive practices, and barriers to preventive practices. We identified the barriers for the nurse population studied and opportunities to overcome these barriers.

Identification and quantification of nitrofurazone metabolites by ultraperformance liquid chromatography-quadrupole time-of-flight high-resolution mass spectrometry with precolumn derivatization.

An ultraperformance liquid chromatography-quadrupole time-of-flight high-resolution mass spectrometry method was developed and validated for the determination of nitrofurazone metabolites. Precolumn derivatization with 2,4-dinitrophenylhydrazine and p-dimethylaminobenzaldehyde as an internal standard was used successfully to determine the biomarker 5-nitro-2-furaldehyde. In negative electrospray ionization mode, the precise molecular weights of the derivatives were 320.0372 for the biomarker and 328.1060 for the internal standard (relative error 1.08 ppm). The matrix effect was evaluated and the analytical characteristics of the method and derivatization reaction conditions were validated. For comparison purposes, spiked samples were tested by both internal and external standard methods. The results show high precision can be obtained with p-dimethylaminobenzaldehyde as an internal standard for the identification and quantification of nitrofurazone metabolites in complex biological samples. Graphical Abstract A simplified preparation strategy for biological samples.

Identification of the -α(2.4) Deletion in One Family and in One Hb H Disease Patient in Guangxi, People's Republic of China.

The 2.4 kb (or -α(2.4)) deletion in the α-globin gene cluster (NG_000006.1) is an α(+)-thalassemia (α(+)-thal) allele. The molecular basis of -α(2.4) is a deletion from 36860 to 39251 of the α-globin gene cluster. It was reported by three research groups in 2005, 2012 and 2014, respectively. In routine thalassemia screening studies by this research group, we found an individual with the -α(2.4)/αα genotype and an Hb H (ß4) disease patient whose genotype was - -(SEA)/-α(2.4). Samples from the parents of the carrier of the -α(2.4)/αα genotype were collected to perform pedigree analysis, and the proband's mother's genotype was diagnosed to be - -(SEA)/-α(2.4). The research revealed that the -α(2.4) allele exists in the population of southern Guangxi, People's Republic of China.

Diagnosis of a Family with the Novel -α(21.9) Thalassemia Deletion.

The Qinzhou α-thalassemia (α-thal) or -α(21.9) deletion was first described at the Qinzhou Maternal and Child Health Care Hospital, Qinzhou, Guangxi, People's Republic of China (PRC) in 2013. The molecular biological mechanism by which this allele leads to α-thal involves the deletion of a 21.9 kb DNA fragment of the α-globin gene cluster (NG_000006.1), designated as -α(21.9). During routine screening, a new family with -α(21.9) was found by the research group. This is the first time that an adult patient with the -α(21.9)/αα genotype and a 6-month-old baby with the -α(21.9)/- -(SEA) (Southeast Asian) genotype were detected in one family. The discovery of this family demonstrates that there is a certain risk for the Qinzhou α-thal deletion in the southern regions of Guangxi Province, PRC. The detection of the adult patient with the -α(21.9)/αα genotype and the analysis of hematological data are important supplements for -α(21.9) research. Additionally, Hb Bart's (γ4) and Hb H (ß4) were detected in the 6-month-old, confirming that the baby with the -α(21.9)/- -(SEA) genotype also carries Hb H disease. The analysis of this family verifies that the -α(21.9) deletion is an α(+)-thal allele.

The diagnosis and molecular analysis of a novel 21.9kb deletion (Qinzhou type deletion) causing α+ thalassemia.

α-Thalassemia is a common single-gene genetic disease that can cause Hb Bart's hydrops fetalis and Hb H disease in tropical and subtropical regions. When examining conventional thalassemia genes, an only detected --(SEA) genotype sample needs further analysis. In doing so, we found a novel 21.9kb deletion (Qinzhou type deletion). The deletion position of the novel 21.9kb deletion is from 14373bp to 36299bp of the α-globin gene cluster (NG_000006.1); thus, there exists a 21927bp sequence deletion, into which a 29bp sequence is added. After sequence analysis, a group of Gap-PCR primers were synthesized to diagnose this novel thalassemia genotype. Through pedigree analysis, we deduced that the propositus obtained the novel alleles from her mother. The genotype of this propositus is --(SEA)/-α(21.9) and its phenotype conforms to the characteristics of Hb H disease, establishing that the combination between -α(21.9) genotype and α(0) genotype can lead to Hb H disease. By molecular analysis, we established that this case fits the characteristic of an α(+) thalassemia genotype.

Role of toll-like receptors in lung cancer.

Lung cancer is a leading cause of death world-wide and the long-term survival rate for patients with lung cancer is one of the lowest for any cancer. Toll-like receptors (TLRs), evolutionarily conserved innate, are expressed in a wide variety of tissues and cell types, and they play key role in the innate immune system. TLRs have been found to be expressed by some kinds of tumor cells. However, what is the biological function of TLRs on tumor cells and whether human lung cancer cells can express TLRs remain to be fully understood. This review was performed to sum up the role of TLRs in lung cancer.

Comprehensive analysis of thalassemia alleles (CATSA) based on third-generation sequencing is a comprehensive and accurate approach for neonatal thalassemia screening.

Thalassemia is one of the most common and damaging monogenic diseases in the world. It is caused by pathogenic variants of α- and/or ß-globin genes, which disrupt the balance of these two protein chains and leads to α-thalassemia or ß-thalassemia, respectively. Patients with α-thalassemia or ß-thalassemia could exhibit a severe phenotype, with no simple and effective treatment. A three-tiered strategy of carrier screening, prenatal diagnosis and newborn screening has been established in China for the prevention and control of thalassemia, of which the first two parts have been studied thoroughly. The implementation of neonatal thalassemia screening is lagging, and the effectiveness of various screening programs has not yet been demonstrated. In this study, hemoglobin capillary electrophoresis (CE), hotspot testing method, and third-generation sequencing (TGS) were used in the variant detection of 2000 newborn samples, to assess the efficacy of these methods in neonatal thalassemia screening. Compared with CE (249, 12.45 %) and hotspot analysis (424, 21.2 %), CATSA detected the largest number of thalassemia variants (535, 26.75 %), which included 24 hotspot variants, increased copy number of α-globin gene, rare pathogenic variants, and three unreported potentially disease-causing variants. More importantly, CATSA directly determined the cis-trans relationship of variants in three newborns, which greatly shortens the clinical diagnosis time of thalassemia. CATSA showed a great advantage over other genetic tests and could become the most powerful technical support for the three-tiered prevention and control strategy of thalassemia.

The population incidence of thalassemia gene variants in Baise, Guangxi, P. R. China, based on random samples.

OBJECTIVE: Thalassemia is a monogenic genetic disorder with a high prevalence in populations in the southern region of China. The thalassemia gene prevalence rate in the Baise population in China is high, and several rare gene variants have been detected in the population of this region during routine testing by our study group. To accurately reveal the thalassemia gene variants carried by the population in Baise, and to provide a basis for the formulation of thalassemia prevention and control policies in the region, we conducted a more comprehensive study in a randomly selected population. RESULTS: In all, 4,800 randomized individuals were recruited for testing from Baise, and the detection of hot spot thalassemia genetic variants were performed by Gap-PCR and PCR-RDB methods, combined with the relative quantification of homologous fragments and AS-PCR to expand the detection range. The prevalence of thalassemia variants in this population was 24.19%, among which 16.69% of individuals carried α-thalassemia gene variants alone, 5.62% carried ß-thalassemia gene variants alone, and 1.88% carried both variants. CONCLUSIONS: The use of positive primary screening combined with hot spot gene variant detection alone can result in a certain degree of missed detection. In the prevention and control of thalassemia in the region, testing institutions need to pay attention to the detection of rare thalassemia gene variants such as αααanti4.2, αααanti3.7, -α2.4, -α21.9, ß-50, ß-90, and ßIVS-II-5, to provide more accurate genetic counseling advice to subjects.

Third-generation sequencing: A novel tool detects complex variants in the α-thalassemia gene.

OBJECTIVE: Thalassemia is a monogenic disorder with a high carrier rate in the southern region of China. Most laboratories currently follow the protocol of testing hematologic indicators in individuals with positive hematologic indicators and then using the hot-spot mutation test kit. A novel thalassemia gene test is performed if there is a mismatch between the hematology and hot-spot mutation test results. However, due to the large population in southern China, some individuals carry complex α-globin gene cluster (CAGC) variants in NG_000006.1, which are difficult to detect using conventional thalassemia genetic analysis protocols, leading to missed or false genetic test results for individuals carrying these complex α-globin gene cluster variants. When an individual carries a complex α-thalassemia gene variant, and an individual carries a ß- thalassemia gene variant, there may be clinical symptoms that might complicate clinical consultation and prenatal diagnosis if not accurately detected. Third-generation sequencing (TGS) enables long-read single-molecule sequencing with high detection accuracy, and long-length DNA chain reads in high-fidelity reads mode. TGS can be used to analyze high homology and rich GC DNA sequences. RESULTS: Four samples that showed abnormalities in the thalassemia genetic test were studied using TGS, revealing that they carried genotypes with complex α-globin gene cluster variants, one of which was a complex variant αα anti3.7 α anti3.7 α 17.2. CONCLUSIONS: TGS detects complex α-globin gene cluster variants. This study may provide a reference protocol for the use of TGS for the detection of complex α-globin gene cluster variants. TGS can reveal individuals with complex α-thalassemia genotypes in the population and improve the accuracy of genetic counseling and prenatal diagnosis.

Parentage analysis using genome-wide high-density SNP microarray.

OBJECTIVE: Parentage analysis is a technology that uses genetic methods to verify or exclude relationships between individuals. STR technology is often used in parentage analysis. We received three sets of samples from three families. Each set of samples consisted of a male individual and a female individual. Their test requirements were meant to determine whether they were a paternity relationship, a sibling relationship, or grandparent-grandchild relationship. However, only one STR locus mismatch was detected in each group. Other family members to assist in testing could not be identified; therefore, other methods were needed to assist in judgment. Using high-density SNP microarrays, we analyzed the feasibility of its application in paternity analysis. RESULTS: A total of 180 samples were tested, including 100 unrelated samples, and 74 samples from 30 families, and six samples from three families. The data were analyzed, grouped according to the chromosome of SNP, and the mismatching rate was counted. The total mismatching rate of SNP in unrelated individuals was 8-10 times higher than that of parent-child individuals. Individuals with a total mismatch rate of more than 5.3% were defined as individuals with no kinship, and the individuals with a total mismatch rate of less than 0.6% were defined as the individuals with a parent-child relationship. CONCLUSIONS: Through the use of high-density gene chips for analysis, we also completed an auxiliary analysis of the kinship of the three families. The gene chip is a better method for auxiliary analysis of the kinship between individuals.

The carriage rates of αααanti3.7, αααanti4.2, and HKαα in the population of Guangxi, China measured using a rapid detection qPCR system to determine CNV in the α-globin gene cluster.

OBJECTIVE: Our study group encountered a pregnant woman whose gene analysis of thalassemia was ß41-42/ßN; however, the patient was severely anemic and had a history of multiple blood transfusions. Further analysis showed that the individual carried the αααanti4.2. Our research group occasionally detected individuals with copy number variations of the α gene, including αααanti3.7, αααanti4.2, and HKαα, but these variations are not within the detection range of conventional gene detection for thalassemia. The purpose of this study was to determine the carriage rate of these α gene copy number variants in the population of southern Guangxi. RESULTS: We used the method of relative quantitative homologous fragments to analyze α1 and α2 genes. 23,900 samples were analyzed. A total of 201 individuals with αααanti3.7, αααanti4.2, and HKαα genes were identified. The carriage rates of these genes in southern Guangxi were 0.39%, 0.29% and 0.16%, respectively. We also collected positive samples from 18 families, and hematology data analysis confirmed that if these individuals carried the ß-thalassemia allele at the same time, would lead to further imbalance of the ratio of α-chain to ß-chain, and then produce varying degrees of anemia. CONCLUSIONS: The individuals carrying αααanti3.7, αααanti4.2, and HKαα genes suffer harms related to ß0 thalassemia, and these variations are not included in the detection range of conventional gene analysis reagents; therefore, these individuals are at risk. Prenatal diagnosis institutions could pay more attention to carriage of copy number variations of α-globin, so as to give more accurate prenatal advice to patients.

Molecular diagnosis of sex chromosome mosaics in fetal amniotic cells.

ABSTRACT: Mosaicism can be observed in karyotype analyses of amniotic fluid cells. Differentiating between true mosaicism and pseudomosaicism and determining mosaic proportions can help avoid misjudgments by doctors and effectively reduce mental and physical harm to pregnant women. However, the detection of mosaicism and mosaic proportions via karyotype analysis and fluorescence in situ hybridization (FISH) is extremely complex. We have developed a novel approach, "segmental duplication quantitative fluorescent PCR" (SD-QF-PCR), to detect mosaicism and mosaic proportions.In this study, twenty control samples and fourteen mosaic samples were tested by first-line karyotype analysis; by second-line karyotype analysis, SD-QF-PCR and FISH were used to reassess fetal sex chromosome mosaicism and mosaic proportions.Detection of the 20 control samples by second-line karyotype analysis via FISH and SD-QF-PCR showed normal and consistent results. Among the 14 mosaic samples, the numbers of samples showing true mosaicism and pseudomosaicism detected by the three methods were 6 and 8, respectively.Our study demonstrates that SD-QF-PCR can be used as a complementary method to traditional cytogenetic analysis of amniotic fluid mosaics and has clinical application value.

Gene-viral cancer therapy using dual-regulated oncolytic adenovirus with antiangiogenesis gene for increased efficacy.

Conditionally replicative adenovirus (CRAD) represents a promising approach for cancer therapy. Several CRADs controlled by the human telomerase reverse transcriptase promoter have been developed. However, because of their replicative capacity, the importance of cancer specificity for CRADs needs to be further emphasized. In this study, we have developed a novel dual-regulated CRAD, CNHK500-mE, which has its E1a and E1b gene controlled by the human telomerase reverse transcriptase promoter and the hypoxia response element, respectively. It also carries a mouse endostatin expression cassette controlled by the cytomegalovirus promoter. These properties allow for increased cancer cell targeting specificity and decreased adverse side effects. We showed that CNHK500-mE preferentially replicated in cancer cells. Compared with a replication-defective vector carrying the same endostatin expression cassette, CNHK500-mE-mediated transgene expression level was markedly increased via viral replication within cancer cells. In the nasopharyngeal tumor xenograft model, CNHK500-mE injection resulted in antitumor efficacy at day 7 after therapy. Three weeks later, it led to significant inhibition of xenograft tumor growth due to the combined effects of viral oncolytic therapy and antiangiogenesis gene therapy. Pathologic examination showed that most cancer cells were positive for adenoviral capsid protein and for apoptotic terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling in the CNHK500-mE-treated tumor tissues, and the microvessels in these tumor tissues were diminished in quantity and abnormal in morphology. These results suggest that, as a potential cancer therapeutic agent, the CNHK500-mE is endowed with higher specificity to cancer cells and low cytotoxicity to normal cells.

2-(2-Hydroxy-ethyl-amino)-3-phenyl-1-benzofuro[3,2-d]pyrimidin-4(3H)-one dichloro-methane hemisolvate.

In the title compound, C(18)H(15)N(3)O(3)·0.5CH(2)Cl(2), the fused ring benzofuro[2,3-d]pyrimidine system is essentially planar [maximum deviation 0.029 (1) Å]. The planes of the pyrimidinone and phenyl rings are nearly perpendicular [dihedral angle = 87.50 (14)°]. The packing of the mol-ecules in the crystal structure is governed mainly by inter-molecular O-H⋯O and N-H⋯O hydrogen-bonding inter-actions and inter-molecular π-π inter-actions between benzofuro[3,2-d]pyrimidine units [the interplanar distances are ca 3.4 and 3.5 Å, and the distances between adjacent ring centroids are in the range 3.64 (1)-3.76 (1) Å]. The dichloromethane solvent molecule lies on a special position.

Generation of adenovirus-mediated anti-CD20 antibody and its effect on B-cell deletion in mice and nonhuman primate cynomolgus monkey.

Therapeutic monoclonal anti-CD20 antibody (Rituxan) is increasingly applied to treat B-cell-related hematologic malignancies and autoimmune disorders with great clinical success, whereas its widespread application is limited by antibody manufacturing capability. Here, we explored a quick and economical adenovirus-mediated anti-CD20 antibody generating system to directly produce anti-CD20 antibody in vivo. We generated a recombinant adenovirus encoding the anti-CD20 antibody gene and found that infection of cells with this recombinant adenovirus led to the generation of anti-CD20 antibody in cells with a similar CD20 binding affinity and specificity as commercial product Rituxan. After one single administration of the anti-CD20-expressing adenoviruses through tail vein at a dose of 1 x 10(9) plaque-forming units/mouse in nude mice, anti-CD20 antibody in the serum was detectable at day 3, reached to the peak value of 246.34 microg/mL at day 14, and maintained a high serum concentration of >40 microg/mL for 56 days. Furthermore, the in vivo generation of anti-CD20 antibody led a complete elimination of preestablished B-cell lymphoma Raji cells in nude mice, and a single administration of the anti-CD20-expressing adenovirus at a dose of 2.0 x 10(9) plaque-forming units/kg in cynomolgus monkey led a continuous B-cell deletion in circulation blood and bone marrow. These observations thus suggest that adenovirus-mediated in vivo generation of anti-CD20 antibody may serve as a new strategy to combat B-cell-related hematologic disorders.

A Shared Decision-Making Tool to Prevent Substance Abuse: Protocol for a Randomized Controlled Trial.

BACKGROUND: Substance use disorder (SUD) affects over 20 million adults and costs over $700 billion annually in the United States. It is one the greatest health care challenges we face. OBJECTIVE: This research project seeks to enhance the standard practice of Screening, Brief Intervention, and Referral to Treatment (SBIRT) through a mobile solution easily incorporated into primary care that will promote shared decision making and increase referral and adherence to specialty care through continued follow-up care. METHODS: This research will conduct an Office of Management and Budget (OMB)-approved randomized controlled trial (RCT) in primary care and SUD specialty service providers. The RCT will recruit a total of 500 SUD patients. Recruited patients will be randomized into control and intervention arms. Both arms will take initial baseline and exit (30 days) surveys to evaluate self-reported substance use and specialty service utilization. The control arm patients will receive usual care. The intervention group patients will receive technology-enhanced SBIRT and a mobile follow-up program to track goals and substance use at home. The RCT tracks participants for 30 days after the primary care encounter. We will collect feedback from the patients during the 30 days and count the number of patients who use specialty care services in specialty care programs for tobacco, alcohol, and drug abuse (both from self-reporting and from the service providers). RESULTS: RCT and data collection are underway. We expect to report the data results in 2018. CONCLUSIONS: We expect that significantly more intervention group patients will receive specialty SUD care within 30 days following the SBIRT encounter at the primary care clinic compared to the control group. We also expect that the intervention group patients will report a greater reduction in substance use and a greater drop in Drug Abuse Screening Test and Addition Severity Index scores within 30 days.